text:
Science on Trial:
On the Biological Effects and Health Risks
Invited Presentation to the Royal Society
following Exposure to Aerosols produced by the use of
Depleted Uranium Weapons
Chris Busby PhD
London, July 19th 2000
Also given in part to the
International Conference against Depleted Uranium
Manchester, 4th 5th November 2000
Occasional Paper 2000/11
[And additional evidence given 12th March 2001]
It is now generally conceded that about 350 tonnes of Depleted Uranium was used in the war and that sub-micron diameter oxide particles became dispersed in the areas that were bombed or strafed. Uranium is known to be a radiation hazard, and radiation exposure is a known cause of all the effects observed in the veterans and the children of Iraq. These facts taken together suggest that the exposure to DU may be the main cause or one of the causes of the observed effects. I will not argue further for the existence of Gulf War Syndrome, or the Iraqi cancer effects in this presentation.
The argument marshalled against this suggestion is that Depleted Uranium is not considered to be a serious radiation hazard since it is so weakly radioactive owing to its long half-life and the fact that its alpha emissions have a very short range. It is argued that on the basis of the 'known relationship between radiation dose and subsequent cancer' the exposure to DU suffered by the Gulf War veterans, or the Iraqi children, cannot have been sufficiently high to be a cause of cancer or mutagenic illness. This is familiar territory to any scientist who has looked into the area of the health risks of exposure to man-made radioactivity: similar arguments are routinely advanced to exonerate radiation as a cause of childhood cancer and leukemia clusters near nuclear reprocessing sites like Sellafield, Dounreay and La Hague, increases in infant mortality and cancer in populations exposed to weapons fallout and fallout from nuclear accidents, cancer increases in nuclear workers and their children, and whole ranges of observations and experience which to most people seem clear evidence of causation. For us, therefore, the questions about Depleted Uranium, are the latest in a long series of questions about the health effects of low level radiation [Busby, 1995].
In the time I have available I want to address four main areas which inform this debate. I will begin by firing my largest cannon. I will show that recent incontrovertible evidence defines the existence of a very large error in the presently accepted model for the health consequences of exposure to low-level man-made radioactivity, and that therefore this same model which underpins the presently accepted assessment of harm from Depleted Uranium, is likely to be similarly flawed. I am tempted to leave it at that. However, it is of some interest to the public, I feel, and should be to the Royal Society, to ask how such a state of affairs could have come about. So I will look and ask if the Scientific Method has been properly used in the assessment of risk from exposure to low-level radiation. We will discover that it has not. Third, I will outline one mechanism which explains how this may have occurred. Finally I will briefly review some of the evidence from the studies of my group which support this new model and show how it applies to the Depleted Uranium controversy.
2. The Chernobyl Infants
I was trained as a chemist. As a chemist, I could stand before you and mix a clear solution of the indicator, phenolphthalein and a clear solution of the base, sodium hydroxide to produce a startling red colour. I cannot hold up a child and mix it with low level radiation to produce leukemia. A very close experiment to this has, however, been recently described and you should be aware of this. It shows, without any doubt, that the concerns of those who argued, either emotionally, or illogically, or with good scientific arguments, that low-level radiation was killing people near nuclear sites, were correct.
Following the Chernobyl accident in 1986, in five different countries, the cohort of children who were exposed in their mother's womb to radioisotopes from the releases suffered an excess risk of developing leukemia in their first year of life. This 'infant leukemia' cohort effect was first reported in Scotland [Gibson et al, 1988], and then in Greece [Petridou et al, 1996], in the United States [Mangano, 1997] and in Germany [Michaelis, et al. 1997]. We first reported increases in childhood leukemia in Wales and Scotland following the Chernobyl accident in 1996 [Bramhall, 1996] but more recently examined the specific infant leukemia cohort in Wales and Scotland [Busby and Scott Cato 2000].
Unlike the earlier researchers, who merely showed the existence of a significant rise in infant leukemia, we decided to examine the relationship between the observed numbers of cases and those predicted by the present radiation risk model. This was an invaluable opportunity since the specificity of the cohort enabled us to argue that the effect could only be a consequence of the exposure to the Chernobyl fallout. There could be no alternative explanation, like the 'population mixing hypothesis' advanced to explain away the Sellafield childhood leukemia cluster. However implausible such theories may be, they have acquired popularity, and their proponents status, as a consequence of their utility to the nuclear lobby. However, 'though population mixing may occur at Sellafield, it cannot occur in the womb.
Because the National Radiological Protection Board had measured and assessed the doses to the populations of Wales and Scotland and because they themselves had also published risk factors for radiogenic leukemia based on ICRP models it was a simple matter to compare their predictions with the observations and test the contemporary risk model. The method simply assumed that infants born in the periods 1980-85 and 1990-92 were unexposed, and defined the Poisson expectation of numbers of infant leukemia cases in the children who were in utero over the 18 month period following the Chernobyl fallout. This 18 month period was chosen because it was shown that the in utero dose was due to radioactive isotopes which were ingested or inhaled by the mothers and that whole-body monitoring had shown that this material remained in the bodies of the mothers until Spring 1987 because silage cut in the Summer of 1986 had been stored and fed to the cattle in the following winter. The result was startling. First, there was a statistically significant 3.8-fold excess of infant leukemia in the combined Wales and Scotland cohort (p = 0.0002). Second, the leukemia yield in the exposed 'in utero' cohort was about 100 times the yield predicted by the model. Table 1 compares the effect in the three main studies. In passing it should be noted that this number, 100, is very close to the error required to explain the Sellafield childhood leukemia cluster.
At this stage we must close another denial exit. It should be noted that the possibility of the effect being due to chance may be obtained by multiplying the p-values for the null hypothesis that the effect was due to chance in each of the separate countries and studies to give an overall p-value less than 0.0000000001. Thus it was not a chance occurrence: it was a consequence of the exposure to low-level radiation from Chernobyl. I am sorry to have to keep banging the gong but I want you to be quite clear about this point.
And since the World Health Organization has given approximate exposure levels in Greece, Germany and the United States, it was also possible to examine the leukemia yield in the infant 'exposed cohort' reported by the several other studies and establish a dose response relationship. This is shown in Fig 1.
It is a curious shape and goes up, down and up again, and this shape should be noted.
Fig. 1. dose-response relationship between exposure to the infants who were in utero at the time of the Chernobyl fallout, and the subsequent risk of leukaemia.
I will return to the shape of this curve below, but first I must ask how it is that some fifty years after the atom bomb, and following a huge amount of research into the subject, we can have discovered such a huge error in the science of radiation risk. To understand the answer, we must look at the scientific method a little more closely.
3. Radiation Risk and Scientific Method
The classical exposition of the scientific, or inductive method (originally due to William of Occam) is what is now called Mill's Canons, the two most important of which are:
Finally to the methods of inductive reasoning we should add considerations of plausibility of mechanism.
These are the basic methods of science [Mill, 1879; Harre, 1985; Papineau, 1996]
Let us first define our question. It is this. What are the health consequences of exposure to novel internal radioisotopes at whole organ dose levels below 2mSv? Because we are looking at battlefield DU, we should add that in this case, although the element is 'natural', the exposure is novel, and due to internal sub-micron Uranium Oxide particles embedded in tissue.
Although risks from exposure to high levels of ionizing radiation are generally accepted, since they are fairly immediate and graphic, the situation with regard to low-level exposure is curious. There are now two mutually exclusive models describing the health consequences of exposure to low-level radiation. There is a nuclear establishment one, which is that which is presently used to set legislation on exposures and argue that DU is safe, and a radical one, which is espoused by the anti-nuclear movement and its associated scientists. I show these two models schematically in Fig 2.
Fig. 2. Mutually Exclusive Radiation Risk Models
The two models arise from two different scientific methods. The conventional model is a physics-based one because it was developed by physicists prior to the discovery of DNA. Like all such models it is mathematical, reductionist and simplistic, but because of this is of great descriptive utility. Its quantities, dose, are average energy per unit volume or dE/dV and in its application, the volumes used are greater than 1kg. Thus it would not distinguish between the average energy transferred to a person warming themselves in front of a fire and a person eating a red hot coal. In its application to the problem at hand, the internal, low-level, isotopic or particulate exposure, it has been used entirely deductively. The basis of this application is that the cancer and leukemia yield has been determined following the external acute high-dose irradiation by gamma rays of a large number of Japanese inhabitants of the town of Hiroshima. Following this, arguments based on averaging have been used (quite spuriously) to maintain that there is a simple linear relationship (in the low-dose region) between dose and cancer yield. This Linear No Threshold (LNT) assumption enables easy calculations to be made of the cancer yield of any given external irradiation.
By comparison, the radical model shown in Fig.2 arises from an inductive process. There have been many observations of anomalously high levels of cancer and leukemia in populations living near nuclear sites, especially those where the measurements show that there is contamination from man-made radioisotopes, e.g. reprocessing plants. In addition, populations who have been exposed to man-made radioisotopes from global weapons tests, downwinders living near nuclear weapon test sites and those exposed to these materials because of accidents (like the Chernobyl infant leukemia cohort) or because of work in the nuclear industry or military. A review of these findings is available [Busby, 1995] and a more recent literature review of studies showing these effects is published by the Low Level Radiation Campaign [LLRC, 2000]. In addition, the radical model is based on biological considerations and considers each type of exposure according to its cellular radiation track structure in space and in time. It is not, therefore, possible to employ this model to predict risks from 'radiation dose' to 'populations' but only from microscopically described doses from specific isotopes or particles whose decay fractionations are considered to interact with cells which themselves respond biologically to the insults and may be in various stages of their biological development. The dose-response relationship following from this kind of analysis might be expected to be quite complex.
These models are at war: which one is correct? What considerations can we use to choose?
The answer is that the conventional LNT model must be rejected because it is not scientific. Its conclusions are based on deductive reasoning. It falsely uses data from one set of conditions, high-level, acute, external exposure to model low-level, chronic, internal exposure. It is scientifically bankrupt, and were it not for political considerations, would have been rejected long ago. On the other hand, it should be clear that the radical model conforms to all the requirements of the scientific method listed above. Man-made radioisotopes, often in the form of 'hot particles' are common contaminants to the areas near nuclear sites where there are cancer and leukemia clusters, and to the downwinders, and to the fallout-exposed populations. This satisfies the Canon of Agreement. The contingency analysis tables with control populations for such studies show that the Canon of Difference is also satisfied: people living in more remote regions than the downwinders show lower levels of illness. We must by now also have some faith in a Principle of Instance Confirmation, since so many studies have shown that increases in cancer and leukemia follow these exposure regimes at low dose. Indeed, the Gulf War Syndrome, might be considered as such an instance confirmation. We are left only with 'Plausibility of Mechanism', which I will address below.
Before I turn to the mechanistic arguments I will try to throw some light on how such a state of affairs continues to go unchallenged by quoting from an eminent and past member of the Royal Society, the Nobel-prize winner, Chemist and Economist Michael Polanyi.
Polanyi, was interested in the scientific method, and in scientists: his writings pre-dated the Science War philosophers like Kuhn and more recently Latour. He was aware that at any time, the scientific world view might be completely wrong. For as Montaigne wrote:
4. Mechanistic Considerations
Averaging Dose
I want to look more closely at the averaging model and its predictions at low dose. It is essentially what used to be called a colligative model: the dE/dM formulation of dose requires that energy transferred from absorption of the consequence of a radioactive disintegration is averaged over the target site, usually the whole body or organ. Whatever lip service is made to considerations of what is now called 'microdosimetry', close examination of calculations done to establish risk near nuclear sites shows this to be the case. The document NRPB R-276, Risk of Leukemia and other Cancers in Seascale from All Sources of Radiation published in 1995 is a good example. In this document, doses to the lymphatic system were calculated by modelling it as 'liver, lung, kidney, spleen, pancreas, uterus and intestines'. A physiologist would not recognise this list as the 'lymphatic system', so why was it used? The answer is that breathing introduces the particles of plutonium that exist in the air near Sellafield into the lungs of the children who live there. From the lungs, these particles are scavenged to the two small tracheobronchial lymph nodes which have a combined mass of perhaps one gram. If NRPB had divided dE by 1 gram, the resultant dose to this part of the lymphatic system would have been extremely high. Given that this organ has been identified as a source of lymphoma and leukemia in animals, this sounds very like the cause of the Sellafield leukemia cluster. But dilution of the plutonium decay energies into the whole mass of guts used for dM reduces the 'dose' to an acceptable small level. This process, incidentally, is very relevant to the DU exposures.
Figure 3 (pending)shows a phantom used by ICRP to calculate doses from external radiation fields. This is the model that is presently used to calculate internal doses. Of course, in the low dose region, cells are either hit or not hit, so the cell dose is very different from the tissue dose. Nevertheless, the model is valid as a means of establishing a quantity, 'dose' which can be correlated with some health consequence like cancer, so long as each cell in the body, or target region, has an equivalent probability of being hit (or more properly intercepted by a track). Dudley Goodhead, a member of the Royal Society depleted Uranium panel, has written of the low-dose region [Goodhead, 1988]:
Cellular responses to radiation: the Burlakova dose response
It has been known from almost the beginning of the radiation age that rapidly replicating cells are more sensitive to radiation damage [Bergonie and Tribondeau, 1906]. Indeed, this is the basis of radiotherapy for cancer where it is the rapidly proliferating cancer cells that are preferentially destroyed. Most cells in a living organism are in a non-replication mode, sometimes labelled G0. These cells are contributing to the organism as part of the normal living process and do not need to replicate unless there is some signal requiring this, perhaps because of tissue growth, damage or senescence. Throughout the growth and lifespan of individual organisms, there is a constant need for cellular replication, and therefore there are always some small proportion of cells which will be replicating: the magnitude will naturally depend upon the type of cell. When cells receive the signal to move out of stasis or G0, they undertake a fixed sequence of DNA repair and replication, labelled G0-G1-S-G2-M, with various identifiable check points through the sequence which ends in replication M or Mitosis. The period of the repair replication sequence is about 10 to 15 hours and the sensitivity of replicating cells to damage including fixed mutation is extremely high at some points during this sequence. This has been known for some time: Fig 4 shows the results of early experiments on Chinese hamster cells indicating up to 600-fold variation in the cell radiation sensitivity over the whole cycle. [Morton and Sinclair, 1966]
Fig. 4. Variation in sensitivity to radiation of Chinese hamster ovary cells over the cell cycle in vitro If we display this response variation on a scale that shows the normal cell lifespan in the organism, rather than just over the cell cycle in vitro, the window of opportunity for cell mutation at high sensitivity becomes apparent Fig 5.
Fig. 5. Displaying the 10 hour repair replication high-sensitivity window in terms of normal cell lifespan in the living organism
So the picture of isotropic dose to equivalent cells, the 'bag of water' phantom model outlined by Goodhead has to be reviewed. Perhaps 1 percent of these cells are actively dividing and are in repair replication sequences that we will assume, for argument, are 600 times more sensitive to being 'hit' by a track. What would we expect the dose-response to look like? Well as the dose was increased from zero, the sensitive cells would begin to be damaged and a proportion of these hits would result in fixing a mutation and increasing the possibility of cancer. As the dose increased further, eventually this rise in response would peak as these sensitive cells were killed. The mutation yield would then begin to fall. However, at some point, the insensitive G0 cells would begin to be damaged and the whole process would begin again, with a rise in cancer. Ultimately there would be a second fall, but this level of exposure would probably result in the death of the organism (although such considerations have been used to explain an observed fall-off in effect from alpha emitters at high dose). So the dose response would look like that in Fig 6.
Fig. 6. Predicted dose-response relationship for mutation in an organism made up of two sub-classes of cell sensitivities: high sensitivity replicating cells and low sensitivity quiescent cells. Sensitive sub-class cells are first mutated (to the left of the dotted line)and then killed as dose is increased (right of the dotted line).
This type of response was shown to occur in several experiments by Burlakova, although she gave a different explanation for it, involving a combination of increasing damage and induced repair curves.
She showed that such an effect can be seen by plotting the results of a large number of separate radiation and leukemia studies, a graph reproduced in Fig 7.
Fig. 7. Leukaemia deaths per 105 person years depending on the dose of radiation. Many different studies plotted (Copied from Burlakova et al. 1996)
The results of animal studies on beagle dogs and mice also show these biphasic effects in the low-dose region [Busby, 1995] . Referring back to the Azande scientists for a moment, it is quite easy to see how such a result might be interpreted as 'hormesis', the radiation-is-good-for-you concept advanced by the nuclear lobby and its scientists. All that is necessary is to plot the biphasic response but leave out the first zero point. The deductive conclusions from high-dose experiments could not be squared with the possibility of such variation in this low dose region so either the points were interpreted as scatter or they were forced into a hormesis dip by leaving out the lowest dose responses as outliers.
Note that this type of biphasic curve is seen in the Chernobyl infant studies collected together in Fig 1.
The Second Event Theory
There is large variation in sensitivity over the cell lifespan. Although naturally dividing cells may accidentally receive a 'hit', this process can be modelled by averaging over large masses of tissue, even if the dose response curve is not linear, as thought. However, unplanned cell division, preceded by DNA repair can be forced by a sub-lethal damaging radiation track: this is one of the signals which push the cell out of G0 into the repair replication sequence. It follows that two hits, separated by about eight hours, can generate a high sensitivity cell and then hit this same cell a second time in its sensitive phase. This idea, the 'Second Event Theory' is described and supporting evidence advanced in Busby 1995 and its mathematical description has been approached slightly differently in Busby 2000. It has been the subject of some dispute by NRPB [Cox and Edwards, 2000, Busby, 2000a]
Very recently, developments in micro techniques have enabled some new evidence that supports the two hit idea to emerge. Miller et al., [1999] in a consideration of Radon exposure risks, have been able to show that the measured oncogenicity from exactly one alpha particle hit per cell is significantly lower than for a Poisson distributed mean of one alpha particle hit per cell. The authors argue that this implies that cells traversed by two alpha particles or more contribute most of the risk of mutation, i.e. single hits are not the cause of cancer.
There are two types of internal exposure for which there would be expected to be an enhancement of risk from this Second Event source. The first, due to sequentially decaying radioisotopes like Strontium-90 has been discussed in Busby 1995, Cox and Edwards, 2000 and Busby, 2000. Following an initial decay from an Sr-90 atom bound to a chromosome, the second decay from the daughter, Yttrium-90, whose half-life is 64hrs can hit the same cell in the induced replication sequence with a probability that is simple to calculate. The same dose from external radiation has a vanishingly small chance of effecting the same process. The second type of Second Event exposure, referred to in Busby 2000a, is from micron or sub-micron sized 'hot particles'. If lodged in tissue, these will decay again and again increasing the probability of multiple hits to the same cell inside the 10 hour repair replication period. It is this process that is relevant to the Depleted Uranium problem.
Second Events from DU particles.
The US Defence Department commissioned research into the levels of Uranium Oxide particulates produced by the impact of Abrams M1A1 Tank ammunition at the Nevada test site in 1986 [USBRL 1986]. The impact on armour of Depleted uranium penetrators results in about 80% conversion to Uranium Oxides UO2 and U3O8 in the form of ceramic particles of diameters in the micron region. These aerosol particles are very mobile and can clearly be inhaled. In this regard the hazard is of a similar nature to that from the Plutonium oxide particles resuspended from Sellafield discharges to the Irish Sea which were considered as a possible cause of the Sellafield leukemia cluster by COMARE and NRPB and referred to earlier where it was recorded that the ICRP66 models used to estimate doses did so by diluting the particles energy into large masses of tissue.
For particles below 1 micron diameter, self absorption of the alpha particle decays may be considered second order and the dose to tissue in the range of these alpha decays calculated. Table 2 shows the calculated doses in spheres of tissue within the 30micron range of the alpha decays.
Table of doses to sphere of tissue 30 micron radius
Assumptions: Uranium Oxide (238U] is in the form U308
Also tabulated is the number of hits per day to this sphere of tissue. The table shows that for particles as small as 0.2 microns diameter, average annual alpha dose to the (lymphatic) tissue surrounding the particles is about the same as the total annual average background dose of 2mSv. For larger particles the dose rapidly increases. Between 0.5 and 5 microns, Second Event processes are stochastically likely. This is shown by Fig 8 where the number of hits per day is plotted against the particle diameter.
Fig. 8. Uranium particle doses to local cell volume: number of hits per day to cell volume from particles of U308 of different diameters.
Fig. 9. Photomicrograph of Plutonium Oxide particle of about 2 microns by 6 microns trapped in lung tissue. Note the alpha star. (Original photo: Robert de Tredici)
Energy density and risk
The consequence of aggregating decays into a small sphere around a 'hot particle' is, of course, that the number of different cells capable of being hit elsewhere is necessarily reduced: we have converted a number of tracks well separated to the same number of tracks close together. If all tracks carry the same risk of mutation in cells in the track, i.e. all hits are equivalent, then there should be no hazard enhancement. The hazard enhancement proposed arises not from some 'hot coal' type of energy concentration process but from the fact that cells may be triggered into a sensitive repair replication sequence which carries a very high sensitivity weighting. It may, of course be true that there would be other reasons why concentrated irradiation of a small cluster of cells could produce unstable cell replication or cell communication fields such as those recently proposed by Sonnenschein and Sato [1999] and this itself may lead to a tumour promotion advantage but this is another matter.
Beta emissions from DU
Before collecting together these considerations there is one further matter which may have been overlooked in the case of DU. Uranium-238 is an alpha emitter but depleted Uranium is also a beta emitter: indeed in the solid form the two beta-emitting daughter isotopes, Thorium-234 (beta; 0.26MeV, 24 days) and Protoactinium-234 (beta 0.23MeV, 6,75 hrs) are in equilibrium with the parent after 20 weeks. These beta emissions are the main radiological hazard in handling the bulk material. In Iraq, I recently measured 24,000 counts per second at the surface of a stray A-10 30mm penetrator which was just lying on the ground. This represented a dose of about 1mSv/hour to the hands of anyone holding the penetrator. However, most of the beta (and alpha) decays were absorbed inside the bulk material, and only surface disintegrations were emerging to be absorbed in the scintillation counter head.
The equilibrium beta activity of DU is about 24MBq/kg. But most of this energy is absorbed in the bulk material: oxidation of the material on impact to produce some 1014 1 micron diameter Uranium Oxide spheres per kilogram would enable all of the decay energy to be potentially available for human exposure. The enhancement of efficiency in release of beta radiation is thus about 1000-fold.
Environmental Mobility of the DU particles
In order to define the population at risk, it is necessary to know the fate of the Uranium particles subsequent to impact. At the Nevada test site, the atmospheric concentration at 100m from impact exceeded the UK NRPB Generalized Derived Limit for Uranium in Air by a factor of about 5 [Busby 1999]. Dietz has reviewed data which establishes that DU particles are able to travel at least 100km from their impact source [Dietz, 1997]. I recently made measurements of alpha radiation levels in Iraq in three areas, the southern battleground near tanks destroyed by DU fire, the same area remote from the tanks, the town of Al Basrah and the city of Baghdad. Results showed that the alpha activity in the battleground area was more than five times higher than in Basrah and ten times higher that in Baghdad. In addition, and remarkably, levels on the surface of the ground near the damaged tanks did not generally show high levels of alpha or beta signal from Uranium and its daughters except in the case of one tank where a yellow contaminant, probably UO3, showed high levels of beta activity. In addition, the insides of tank turrets which had radioactive holes in them from A10 hits, did not show high levels of beta or alpha activity. The generally higher alpha levels in the whole area, coupled with these observations suggest that the Uranium particles has been efficiently dispersed by some mechanism. I believe that this mechanism is the repulsion of charged particles by themselves and by the earths permanent electric field of 150V/m. I have argued elsewhere that this effect operates in the Kennet Valley near the Atomic Weapons plant at Aldermaston and results in the preferential concentration of charged radioative particles near electrostatic discontinuities between strata with different conductivity [Busby, 1997] . A similar effect near high voltage power lines was recently found by Henshaw et al. [1999].
Conclusions on Mechanism
Thus we can conclude that the external bag-of-water model is not an accurate representation of the kind of processes that occur at the cellular level and that the physics based descriptions do not apply to internal irradiation. The Uranium Oxide particles are capable of travelling very large distances [Deitz, 1997]. They may then be inhaled and will become trapped in the lymphatic sytem where they may be transported to any part of the body. Here they may cause sequential moderate dose irradiation of local tissue volumes where the risk of mutation is far higher than is suggested by the LNT and average dose models.
The enhancement of mutation efficiency that follows from exposure to inhaled Uranium oxide hot particles is capable of explaining what might be thought of by Michael Polanyi's Azande scientists as 'anomalous responses to low dose exposure'. We are not, however, reduced to looking only at the Gulf War Syndrome and the Iraqi children for supporting evidence. There are other indicators, and our springboard for these is the 1983 observation of a childhood leukaemia cluster at Sellafield. In the last four years Green Audit been funded by the government of the Republic of Ireland to study cancer incidence close to the Irish sea. The study has used both Wales Cancer Registry and Irish Cancer Registry data to examine and explain variations in cancer risk with distance from the sea. The results of this work will be published elsewhere but since they cast considerable light on the DU problem, some of the findings will be briefly reviewed here.
5. Sea coast cancer risks and resuspended hot particles.
In three separate investigations between 1997 and 2000, Green Audit discovered profound and statistically significant evidence of excess risk of cancer incidence and mortality in coastal populations in Wales, Ireland and Somerset. The excess risk has been found for most of the cancer types and sites and in the following data:
As one example of the type of result found, the all malignancy relative risk for populations of all ages in Wales from 1974-89 is shown plotted against distance from the Irish Sea in Fig 10.
Fig. 10. All malignancy incidence relative risk (base population England plus Wales 1979) for populations of Mid and North Wales 1974 - 1989 all ages by distance from the Irish Sea in km. (LOESS fit)
Note the sharp rise in risk near the coast. Sufficient evidence has now accumulated from these studies to support the hypothesis that this cancer risk is a consequence of an exposure route involving inhalation of resuspended radioisotopes, particularly Plutonium Oxide particles. The trend in concentration of Plutonium with distance from the sea in Cumbria has been established and is shown in Fig 11.
Fig. 11. Inland penetration of Plutonium in air and seaspray (Eakins and Lally)
The radioactivity is brought inland by seaspray scavenging mechanisms which are quite well understood: indeed, the ocean is the source of about 30% of all PM10 particles in the UK. It is therefore not surprising that NRPB workers found Plutonium in the tracheobronchial lymph nodes of autopsy specimens from all over the UK in proportion to their distance from the west coast, particularly Cumbria [Popplewell, 1986]. Table 3 shows some results of these studies, which were, incidentally, omitted from the considerations in the COMARE report on the Sellafield leukemia cluster. Nor is it surprising that Plutonium is found in children's teeth in the UK at levels which reflect a similar trend with distance from the Irish Sea [Priest et al, 1996]
Table 3. Plutonium in autopsy specimens from UK (Popplewell NRPB)
6. Overall Conclusions
The Gulf War Syndrome and the increases in cancer and congenital effects in Iraqi populations are merely more and recent evidence of the serious error in the way in which the health consequences of ionizing radiation exposures are presently modelled. They do not stand alone as some sort of curiosity which needs special examination and complex explanations. Polanyi's Azande scientists might have to find some special explanation here: perhaps their Oracle would tell them that the problem must be that the Gulf War veterans had been given many injections to protect against gas attacks by the evil dictator. But then they would have to have another explanation for the Iraqi children who did not receive such injections. So their problems have to be something else, perhaps the oil well fires. But then, what about the children in the north, who were also bombed but there was no oil? Perhaps, in that case, it was a demon: population mixing. Or maybe there is no increase in illness and the evil Iraqis have made it all up. Quick! Despatch a team from IARC in Lyon to discover that the Iraq Cancer Registry only has a 286 computer (this happened). Ah! That must be it. A computer problem. And so forth.
In this affair, it is not DU that is on trial. Science itself is On Trial, and the Royal Society is On Trial. If this committee follows the Azande method of deliberation, the credibility of the Royal Society will be finished. Because, following the Azande Scientific Oracle advice on BSE, Global Warming, Sellafield, Mobile Phones and GM crops, it would take very little for people to revert entirely to believing the evidence of their own senses and the advice of their own instincts in areas that to their unscientific minds appear both massive and vital.
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Henshaw, D.L, Fews, A, Keitch, P, Close JJ, Wilding, RJ (1999) Increased Exposure to Pollutant Aerosols under High Voltage Power Cables International Journal of Radiation Biology 75/12:1505-21
LLRC, (2000) see the website www.llrc.org/compendium.htm
Mangano, J. (1997), Childhood leukemia in the US may have risen due to fallout from Chernobyl, British Medical Journal, 314: 1200
Michaelis J, Kaletsch U, Burkart W and Grosche B, (1997) Infant leukemia after the Chernobyl Accident Nature 387, 246
Mill J.S (1879) A system of Logic (London: Longmans Green)
Miller R.C, Randers-Pehrson, G Geard, C.R, Hall, E.J and Brenner, D.J (1999) The oncogenic transforming potential of the passage of single alpha particles through mammalian cell nuclei. Proc. Natl. Acad. Sci. USA 96: 19-22
Papineau D (ed) (1995) The Philosophy of Science Oxford: University Press
Petridou, E., D.Trichopoulos, N.Dessypris, V.Flytzani, S.Haidas, M.Kalmanti, D.Koliouskas, H.Kosmidis, F.Piperolou, and F.Tzortzatou, (1996) Infant Leukemia after in utero exposure to radiation from Chernobyl Nature, 382:25, 352
Priest, N. D., ODonnell, R.G., Mitchell, P. I., Strange, L., Fox, A., Henshaw, D. L., and Long, S. C. (1997), Variations in the concentration of plutonium, strontium-90 and total alpha emitters in human teeth collected within the British Isles, Science of the Total Environment, 201, 235-243.
Popplewell, D.S (1986) Plutonium in Autopsy Tissues in Great Britain Radiological Protection Bulletin No 74 Chilton: NRPB
Sinclair, W. K. and Morton, R. A. (1966), X-ray Sensitivity during the Cell Generation Cycle of Culture Chinese Hamster Cells, Radiation Research, 29: 450-74.
Sonnenschein C and Sato A (1999) The Society of Cells (Harvard: University Press)
If you are seeing this page full screen (i.e. without a navigation bar on the left) you can't see how the rest of the site is organised.
Aberystwyth: Green Audit
October 2000
1. Science on Trial: the Health Effects of Low Level Radiation
The Royal Society Committee on Depleted Uranium has been set up, as I understand it, to evaluate the health risks associated with the battlefield use by the military of the armour-piercing penetrators manufactured from this material. The question of the possible risks to the health of those who were exposed to it has now arrived at the door of this august body, the Royal Society. This is because it has sequentially passed through the stages of being addressed by several other less grand committees of experts whose job it is to know about these things, but who have all answered the question in a way that is not believable, given the real world data, what we might hesitantly label 'the facts'. The facts are that veterans of the recent Iraqi war have been suffering from a mysterious ailment called 'Gulf War Syndrome' which has all the indications of a consequence of chemical or radiation poisoning. The cancer rate in particular has sharply increased in this group of people suggesting exposure of the soldiers to a mutagen, or carcinogen. In addition, the population of Iraq in the areas where DU weapons were used seems to be suffering a similar fate, but in these territories also there have been reported increases in childhood cancer and malformation rates, again indication of a mutagen source.
Wales and Scotland
Exposed cohort B
unexposed cohort A+C
Risk ratio B/A+C
p-value (poisson)
Estimated dose microSv
Horizontal axis = dose (mSv): vertical axis = leukaemia risk
Data points from left:- United States, England, Scotland, Wales, Germany, Greece
The Canon of Agreement which states that whatever there is in common between the antecedent conditions of a phenomenon can be supposed to be the cause, or related to the cause, of the phenomenon.
In addition, the method relies upon the Principle of Accumulation which states that scientific knowledge grows additively by the discovery of independent laws, and the Principle of Instance Confirmation, that the degree of belief in the truth of a law is proportional to the number of favourable instances of the law.
The Canon of Difference which states that the differences in the conditions under which an effect occurs and those under which it does not must be the cause or related to the cause of that effect.
study group
Type of exposure
Analytical approach
Resulting model
A-bomb survivors
High dose
DeductiveLinear No Threshold
(Low risk)
Nuclear site leukaemia clusters (e.g. Sellafield)
Irish Sea coast effect
Chernobyl infants
Minisatellite mutations
Weapons fallout cancers
DU Gulf veterans
Iraqi children
InductiveBiphasic cell response
(High risk)
The Royal Society committee is invited to apply these considerations to the responses which followed the discovery by Yorkshire TV of the childhood leukemia cluster near Sellafield, and bear them in mind whilst deliberating the effects of DU.
Since a wise man may be wrong, or a hundred men, or several Nations, and since even human nature, as we know it, goes wrong for several centuries on this matter or on that, how can we be certain that it occasionally stops going wrong and that in this century it is not mistaken?
In asking how we know anything at all and how we build up a picture of the 'real world' Polanyi saw many similarities between scientists and primitive witch-doctors like the Azande who had been studied by the anthropologist Evans Pritchard who wrote:
(Montaigne 1533-92, The Essays)
They reason excellently in the idiom of their beliefs, but they cannot reason outside, or against their beliefs, because they have no other idiom in which to express their thoughts. The contradiction between experience and one mystical notion is explained by reference to other mystical notions.
For the scientific world view, Polanyi concluded:
E. Evans Pritchard, Witchcraft, Oracles and Magic among the Azande, 1937
[For] the stability of the naturalistic system we currently accept, instead, rests on the same logical structure as Azande witchcraft beliefs. Any contradiction between a particular scientific notion and the facts of experience will be explained by other scientific notions. There is a ready reserve of possible scientific hypotheses available to explain any conceivable event. Secured by its circularity and defended by its epicyclical reserves science may deny or at least cast aside as of no scientific interest, whole ranges of experience which to the unscientific mind appear both massive and vital.
M. Polanyi FRS, Personal Knowledge, 1958
Most situations of practical interest are characterised by cells receiving occasional single tracks well separated in time from any other tracks which may impinge on the same cell. From Natural Background, there is, on average, about one track per year through each cell nucleus. Therefore it is highly unlikely that there will be multiple tracks in short times (< 1 day) over which repair of radiation induced damage within cells is usually observed to take place.
It is these (essentially external irradiation) considerations that enable the model to assume the linear dose response relationship that is the basis for radiation risk. But there are two situations of practical interest that Goodhead's arguments do not address. The first is that a cell's response to radiation damage is not constant over its lifespan: cells are very sensitive to radiation when they are in their repair and replication cycle. The second is that for internal radionuclide decays, either from sequential emitters or from 'hot particles' the microscopic local radiation flux, or energy density, may be very high, even though the average dose may be low. For internal exposure, these are common situations. Here the concept of 'dose' no longer applies and the conventional model breaks down. I will address these in turn.
(Sinclair and Morton 1966)
Horizontal axis: time in hours; Vertical axis: Vertical axis is fraction of cells surviving the radiation.
Upper line: 660 rads; lower line: 1000 rads
1% of cells are actively dividing and 200 - 600 times more radiosensitive than non-dividing cells.
Horizontal axis = dose: vertical axis = effect
by one particle of U3O8 of various diameters 7
Particle diameter microns
Particle volume cm3
Mass U308(g)
Mass U238(g)
Activity of particle (Bq)
Hits /day(dose mSv)
Hits/year(annual dose mSv)
4.2 x 10-15
3.6 x 10-14
3.06 x 10-14
3.8 x 10-10
3.3 x 10-5
(3.96 x 10-3mSv)
6.5 x 10-14
5.6 x 10-13
4.8 x 10-13
5.9 x 10-9
5.1 x 10-4
5.2 x 10-13
4.3 x 10-12
3.7 x 10-12
8.8 x 10-8
7.6 x 10-3
4 x 10-12
3.5 x 10-11
2.9 x 10-11
3.6 x 10-7
6.5 x 10-11
5.6 x 10-10
4.75 x 10-10
5.9 x 10-6
(density = 8.6);
specific activity of 238U = 12.43 MBq/Kg;
Alpha decay energy = 4.45MeV;
Alpha range = 30 microns.
Relative Biological Effectiveness factor for Alphas = 20 (from ICRP) has been used to convert dose in Grays to effective dose in Sieverts.
These 'hot particle' processes have been known about for a long time: Fig 9 shows a radiographic photomicrograph of a plutonium oxide 'hot particle' in lung tissue. Overlapping tracks can be seen.
Horizontal axis = U308 particle diameter in microns: vertical axis = hits per day
light line is number of hits after allowing for the self absorption of energy within the particle itself
Incidence data for small areas in Wales from Wales Cancer Registry from 1974-89
In each area the trend with distance from the sea shows a sharp rise in the group of people living within 800m of the sea coast. It is driven by proximity to areas of intertidal sediment known to be contaminated with radioisotopes from Sellafield discharges. In the case of the Somerset study, which was investigated as a hypothesis test the drying, offshore, mud bank, known as the Steart Flats, was contaminated by historic releases from the adjacent Nuclear Power site at Hinkley Point.
Incidence data for small areas of Ireland from the Irish National Cancer Registry for 1994-1996.
Mortality data for census wards in Somerset from the Office for National Statistics for 1995-1998
Horizontal axis = distance from sea in Km.: vertical axis = Relative Risk
Horizontal axis = Distance downwind from sea (Km):
vertical axis (upper figure) = Relative concentration of 239,240Pu in air (pCi m3): lower figure Concentration of 239,240Pu (pCi g-1Na)
Tissue (post mortem)
Cumbrian workers
(Figures given for each of three cadavers in mBq/Kg Pu)Cumbrian public
(mBq/Kg Pu.
Figure in brackets is number of cadavers) Public elsewhere
(mBq/Kg Pu.
Figure in brackets is number of cadavers)
949 (10)
6 (43)
1005.4 (11)
3.6 (35)
1206.8 (11)
1.9 (47)
Tracheo-bronchial lymph nodes
160035 (12)
10 (37)
Pu in various organs at post mortem from members of the public and from occupationally exposed workers living in Cumbria (mBq/Kg)
Radioactive Times report
Additional evidence given to Royal Society Working Group 12th March 2001
This Home page link takes you to the index page, which has links to all the topics we discuss on the site [only use it if this page is full screen]
Use the Depleted Uranium button to see what else we have to say on this topic.
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subset: commoncrawl


text:
Topic: Soptic
Crossroads Ad Pushes Obama to Condemn Steelworker Ad
There's a danger in hitting back against wild, unsubstantiated accusations. Do it wrong, and you can end up bringing more attention to the initial smear, i.e. "Congressman Denies Beating His Wife." But American Crossroads hits the right notes in its latest ad, contrasting the honorable rhetoric of 2008-Obama with the mud-slinging in the Priorities USA steelworker ad. The powerful audio at the end is a great touch (former White House counsel John Dean speaking on the Nixon White House tapes in 1973, informs Mike Allen):
The Romney campaign is also increasing pressure on the Obama camp to denounce the ad. In an interview with Bill Bennett yesterday, Romney tore into the president's campaign:


text:
No, your eyes are not deceiving you. There were two winners, she shares the win with DJ Paul Kom. The VH1 Reality Show gave contestants the challenge to design name and open a restaurant in a few weeks. The two will be partners in the restaurant they launched in Los Angeles, owned by Mike Malin (Boogie from "Big Brother)
The Real Housewives of New Jersey alum did keep her eye on the prize throughout the contest, despite various breakdowns and angry exchanges. Of the contestants, she was less dysfunctional than her fellow castmates, including the useless Heidi Montag, pretty boy Jake Pavelka, and Vincent Pastore (Big Pussy from 'The Sopranos).
What do you think of the Danielle Staub win?vg
One Response to "Danielle Staub Wins Famous Food"
Good for Danielle! She was screwed over by Andy Cohen and the Manzo-Lauritsa mob on RHNJ….she deserves some good to come out of a reality show.
Sorry, the comment form is closed at this time.


text:
My Italian is a little rusty, so I hope I got the title right. Either way, here's what I was referring to:
Isn't that gorgeous? It's Italy, of course, seen on August 18, 2012, at night by astronauts aboard the International Space Station. The ISS was well to the southeast, probably over Libya or Egypt in Africa, when the astronaut took this shot facing northwest. I poked around a bit, and the ISS was in this position twice on that date. Once was during the day, and the other around local midnight, so that fits.
It's pretty neat to see Italy from space; I've posted an image like this before (though the ISS was much more overhead for that one). In this one you can see the arc of green airglow caused by oxygen atoms about 100 kilometers up giving up energy after getting whacked by ultraviolet light from the Sun. To the left and along the top you can see some of the ISS structures, too.
I'll note that on Thursday, August 23, NASA announced that the private company SpaceX had been approved for a dozen cargo flights to and from ISS; this comes after their successful demo mission in May. The first of these flights is scheduled for October 2012. Not only that, but the aerospace company XCOR will be opening a new facility in Florida, near NASA's Kennedy Space Center. XCOR is building a reusable suborbital spaceplane called Lynx, and expects to phase into orbital work eventually.
It's exciting to see private industry getting involved! And it shows that, when it comes to space travel, America is still looking up.
Image credit: NASA. Tip o' the spacesuit visor to Fragile Oasis.
Related Posts:
– Buonanotte, Italia
– The softly glowing night sky
– Turns out, it *is* a river in Egypt
– Debating space


text:
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Telescope, Standing tripod
The Barska 15-45x50 Anchormaster with Floor Tripod is powerful yet elegant. It features 15x to 45x variable-zoom magnification power and 50mm objective lens diameter. Part of Barska's timeless Classic Connoisseur collection, the Anchormaster telescopes express traditional sophistication with exquisite mahogany and brass construction. The precision-made optics are in a class by themselves, as functional as they are beautiful. They boast fully coated achromatic lenses for crisp, brilliant images, and have been structured in a refractor design with helical focusing rings. Brass mounts allow you to move the scope smoothly in all directions. This telescope comes complete with a standing mahogany tripod that has extendable legs and polished brass joints. It is ideal for both celestial and terrestrial viewing.
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Q1: I want to make sure that when I purchase this scope or one similar that it will not view things upside down, will not be using for star gazing.
A: The Barska 15-45x50 Anchormaster Brass Telescope will view everything right-side up.
Don't see the answer you need? Ask a Product Expert! The answer will be emailed to you and then posted here.


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text:
Is papyrophobic!
Posts: 1,926
Karma: 1009999
Join Date: Aug 2003
Location: USA
Device: Dell Axim
The Fuss About Gmail and Privacy: Read why it's Bogus
There has been a rash of recent editorials about privacy concerns with Google's gmail service. A number of organizations have asked Google to voluntarily suspend the service. One California legislator has gone so far as to say she plans to introduce a bill to ban it. This is nuts!
...says Tim O'Reilly from the famous O'Reilly Media publisher. Well, I did read his nine arguments, actually twice (!), but I cannot agree with him. "Gmail is fascinating to me as a watershed event in the evolution of the internet. In a brilliant Copernican stroke, gmail turns everything on its head, rejecting the personal computer as the center of the computing universe, instead recognizing that applications revolve around the network as the planets revolve around the Sun." To me it sounds as if Tim was among those celebrities like Arnold Schwarzenegger, Henry Kissinger, Shaq O'Neal who put money into Google in 1999 through Angel Investors. Now he might be waiting for the big bucks in return. Would you want your mail being scanned by a bot for commercial purposes? |
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text:
In the World of Women-A dark vision of the future
Lord of Mayhem
Dark Fantasy,
Author's infos
Gender: male Age: N/A Location: N/A
Posted Thu 8th of December 2011
Do you REALLY think the world would be different if women ran everything? Some things never change.
Day 1
The young Asian sentry paces her rounds, rifle slung over her shoulder. It's almost 4 A.M. and almost the end of her watch, and she can't wait to get out of her boots and into her nice warm bunk! A 17 year old regular infantrywoman, she is on guard here at army headquarters in a quiet sector of the devastated city, and the battle has shifted elsewhere. There's not an enemy soldier anywhere near here she reflects happily, and a smile creases her pretty face as she continues her pacing, secure in the knowledge that she will not be staring death in the face this day as will so many of her comrades.
The sentry never hears the stealthy approach of the hunter emerging from the shadows. Her eyes open wide in amazement as the hand reaching out from behind her clamps firmly over her mouth, and she feels the agonizing sear of the razor sharp knife burning into her throat. In disbelief, she sees the red jet shoot out from her throat as it is slashed from ear to ear in one seamless cut. All goes black as the hand is withdrawn from her mouth, allowing her already lifeless shell to drop heavily to the ground, the still wide open eyes now staring into oblivion, as the red pool gushing from her throat grows larger.
The Blonde trooper, her blood reddened knife still in her hand, motions her fellow soldiers forward. Stealthily creeping forward, the two platoons of Blondes cautiously fan out and deploy in attack position in front of their objectives. The two platoon corporals will lead the assault with ten troopers ; the sergeants, Amy and Karen, hang back with a reserve of ten more troopers, alert to any unexpected countermoves made by the enemy. This is too easy, thinks Amy's platoon corporal, Katie. Only one sentry? This has got to be some kind of trap! Katie nods to her fellow corporal, and then moves forward with five of her troopers. They will neutralize the barracks first. Without expecting it to open, Katie tries the door to the barracks, and is shocked when it pushes open under her hand. Their security is pathetic! she can't help but think to herself. The snug warmth generated by the sleeping bodies of 19 young human females caresses Katie's face as she sticks her head into the darkened barracks. They're all asleep, she thinks joyfully. Surprise is complete. Katie and her troopers position themselves around the bunks of their sleeping enemies, allowing a brief moment for their eyes to adjust to the darkness. At a signal from Katie, the carnage begins. The first half dozen Asian infantrywomen never wake up. Huddled fast asleep in their blankets, some in their panties, others (against regulations) completely nude, their dreams are cut brutally short and they are sent spiraling into the eternal darkness as three quick, savage bayonet thrusts delivered to each of their bodies extinguish their lives. Even as they fall into the arms of death, blood continues to flow from their destroyed young bodies, saturating the blankets that will serve as their funeral shrouds. The Blondes now move quickly to eliminate their remaining enemies.
The 17 year old Asian infantrywoman is in deepest sleep, her beautiful young body with its perky breasts deliciously naked in her blankets. Under the covers after lights out, she wiggles her way out of her ungainly regulation issue panties, and delights in the feel of her completely naked flesh against the sheets on her bunk. It's against regulations to sleep in the nude, I know, she muses, but nobody checks on us anyway. She is deep in an explicit, erotic dream when to her frustration the dream dissolves and she slowly begins to surface from her pleasantly heavy slumber. Some outside force is pulling her out of deepest sleep. Groggily, her first blurred, semi-conscious thought is how wet her pussy is. That was some dream I was having! And to wake up right in the middle of it! Her hand slides down below her waist and she is just about to insert a finger into her yearning young womanhood, when her expanding consciousness pulls in the sound of commotion, of movement in the barracks, and could she have really heard it? A muffled groan? Her sleep heavy eyelids are just on the verge of forcing themselves open, when the blow hits her in the stomach with brutal force as the bayonet slashes through her blanket and its razor sharp blade, already glistening with the blood of a prior victim, slices into her flesh. She can feel the blade quickly being withdrawn, and can feel the flow of blood escaping from the opening it has created, followed by the hellish pain that seizes hold of her entire body. Eyes now wide open, she opens her mouth to scream, but the scream dies in her throat as a second bayonet thrust punctures her heart. Her body's engine gives one last feeble sputter and she can feel the third and final thrust of the bayonet brutally slam into her body even as life is extinguished and she drops into the abyss of eternal darkness.
The blood is now completely soaking through the blankets and seeping into the thin mattresses on the bunks of the slaughtered infantrywomen as Katie advances towards the last two remaining bunks at the far end of the barracks. All of the occupants of the other bunks are now deep in the sleep of oblivion. As Katie nears the bunks of the two survivors, a terrified young Asian, clad only in panties, scrambles out of the bunk, holding her arms high in the air. Covering her with her rifle, Katie orders one of her troopers, "Get her out of bed," indicating with a nod the still fast asleep occupant of the last bunk. The Blonde trooper flings back the blanket and brutally yanks the recumbent figure out of bed. Presently, blinking her sleepy eyes and groggily trying to comprehend what is happening, this second young infantrywoman, also clad only in her panties, is standing next to her comrade. "OK, let's clear out of here," orders Katie, and escorting their two prisoners, the Blondes exit the barracks. As the last trooper shuts the door behind her, she can hear a faint, soft splashing sound. The blood of the slain infantrywomen, having soaked completely through their thin mattresses, is now beginning to drip onto the floor beneath the bunks.
The young Asian infantrywoman now lies on her back, her mouth and unseeing eyes both frozen wide open, her naked flesh now growing cold, as blood oozes out of her deep bayonet wounds. Her interrupted erotic dream is now not even a memory, her consciousness obliterated along with her life. Soon, they will come for her and mercifully cover her contorted face with the blood soaked blanket. With her pretty bare feet peeking out from under the blanket, she will be carried out of the barracks and laid on the cold, hard ground outside, her toes pointing at the open sky. Later, she will be placed side by side with her comrades in a long trench and covered with earth. All trace of her existence obliterated, the only fleeting reminder of her young life is the blood stained pair of panties she had slipped out of the night before, now lying on the floor of the barracks next to her bunk.
The operation is a success. "Good job taking out that sentry, trooper," Amy praises Linda, the quiet, beautiful blonde who had slit the young sentry's throat without giving it a second thought. The Blondes have seized their objective and have suffered no casualties. The only source of disappointment is when Karen's corporal emerges from the General's quarters and announces, "The General's not here, sarge." The General's capture had been a key objective of this operation. What will headquarters say, when they learn that she has escaped?
Five prisoners are lined up before Amy and Karen. One of them is an Asian Captain, standing proudly erect in her smart black uniform coat and skirt, with highly polished black patent leather boots. She had been captured in the command post while her infantrywomen were being slaughtered in their bunks. "Where's your General?" Amy asks the Captain. "She left last night," comes the reply. "Where did she go?" Amy persists. "That is all I will tell you," the Captain replies contemptuously. "We won't get anything more out of her," Karen interrupts the impromptu interrogation. "I'll have two of my troopers escort her back to headquarters. They'll interrogate her there and then process her out." Two members of Karen's platoon step forward and escort the Captain away. "Let me get my platoon squared away. You can deal with the rest of these prisoners," Karen tells Amy cheerfully, and begins rounding up and reorganizing her platoon.
Amy and Katie survey the four remaining prisoners. Two are the infantrywomen, the only survivors of the slaughter in the barracks, standing before their captors in nothing but the panties they had been captured in. According to the birthdates on their identity tags, both are 17 years old. Those regulation panties are so unattractive, Amy can't help but think to herself. These girls would look so much better in little lacy undies. The other two prisoners form a remarkable contrast. They are both dressed in the tightly fitting uniform coats and skirts of the Asian Cadet Corps, their feet shod in high heels. High heels in a war zone! Amy shakes her head. The cadets, captured along with the Captain in the command post, are even younger than the infantrywomen. Both are only 15. "Are we sending them back to headquarters?" Katie asks. "No, of course not. We'll just process them out right here," replies Amy. "Them too?" Katie asks, indicating the cadets with a nod of her head. "Of course. Why wouldn't we process them out?" Amy replies, almost incredulously. "Well, they're so young, plus they're just staff girls," reasons Katie. "They're old enough to be in uniform, so that means that they're soldiers, and since they're soldiers, they get processed out," Amy responds firmly. "The enemy does the same to our young girls." Amy looks again at the prisoners. They're all such pretty girls. It is a shame, but war is war, she thinks to herself, looking quickly away as she sees tears standing in one of the cadet's eyes. "Bullet or bayonet?" Katie now asks, abandoning her efforts to save the cadets. "Bayonet," replies Amy. "We don't want the enemy to know we're here. Two at a time. Detail Janine and Donna to process them out."
"I know you feel sorry for those cadets, but you do realize that if we send them to headquarters, they'll just be processed out anyway?" Amy asks Katie, pulling her off to one side. "I know," Katie replies hesitantly. "But you wanted to give them another 48 hours of life, didn't you?" Amy gives voice to Katie's unspoken motive, and Katie nods affirmatively in response. "All that would happen is they would get their hopes up that they were going to be spared, and they would both just end up getting a bullet through the heart anyway. Believe me, it's much less cruel this way," Amy reassures her corporal. "Go do what you have to do, corporal," Amy now says decisively. "Yes, sarge," replies Katie. "And remember, follow regulations. Regulations state that all prisoners must be fully stripped before being processed out." "Yes, sarge," Katie replies again and turns to go. What a silly regulation, to have them stripped like that, thinks Amy as she watches Katie go. Who came up with that regulation anyway? Sounds like something a man would dream up.
Katie now stands in front of the platoon with the two troopers selected to process out the prisoners. Donna is an attractive, large breasted girl of average height, considered somewhat slow witted by her troopers, but a reliable soldier none the less. Janine is petite and stunningly beautiful, but beneath her angelic features lies a deep streak of cruelty that makes her the perfect killer in the eyes of her sergeant. The Blondes, dressed in their neat olive drab fatigues, bayonetted M-16s at their sides, face the four prisoners. "The prisoners will strip!" Katie calls out, beginning the processing out.
The 15 year old cadet heaves a sigh as she unbuttons her uniform coat. Glancing to her side, she sees her fellow cadet starting to strip off her own uniform, and the two infantrywomen pulling their panties down to their ankles and stepping out of them. The cadet takes off her jacket, neatly folds it up, and places it on the ground at her feet. Spring is in the air, and as she begins to unbutton her blouse, her mind flashes back to her girlhood. She remembers the fresh spring air, the scent of flowers and the sound of birds singing in her parents' garden. There is no life here, she reflects. No flowers, no birds. Only death. As she pulls off her blouse, revealing a lacy pink bra, she steals a quick, admiring glance at the two naked infantrywomen, noting with approval the long, luxuriant jet black hair, beautifully rounded young ass cheeks and the firm perky breasts, their nipples erect from the chill in the early spring air. We are all so young, and soon we will all be devoured by death. Our flesh is nothing but food for death. She slips her feet out of her high heels and the ground feels cold beneath her now bare pretty little feet with their pink painted toenails. She glances over at the inert forms of the dead infantrywomen lined up for burial, bare feet poking out from under blood soaked blankets, and realizes that soon, she will be sharing a common grave with them in this same cold, unforgiving ground that lies beneath her feet. She is surprised that she does not fear the thought. I will not be alone, I will be sleeping with all of them, she reassures herself comfortingly. She unhooks her skirt, lets it drop to her feet and steps out of it, revealing a pair of pink lace panties that match her bra. She gives another quick glance at her now bare breasted fellow cadet and can't suppress a little smile on catching sight of the thong underwear her comrade is wearing. She always was a wild one, she giggles to herself, as she unhooks her bra, freeing her own young, firm pair of breasts. Finally, she slides her panties off her ass, down her thighs, and yet further down past her knees to her ankles, and steps out of them. She now stands as naked as the day she was born, and gazes once again at her now equally naked fellow cadet. The girls lock eyes for a long moment. Be brave, her eyes implore her friend. It will all be over in a moment. The Blonde corporal orders the two cadets to stand side by side. They will be the first to be processed out.
It is now time. At a shouted command from the Blonde corporal, the two troopers step forward, advance toward the cadets, and stop several paces in front of them, resting the butt ends of their bayonetted M-16s on the ground at their sides. A third trooper quickly moves behind the cadets and ties their hands behind their backs. The young cadet looks down one last time at her feet and wriggles her toes, with their pretty pink toenails. Looking up again, she takes a closer look at the Blonde trooper standing before her. The trooper is the shorter of the two Blondes. She's so petite, thinks the cadet. And very, very beautiful, the cadet can't help but think as she gazes in admiration at the woman who will be processing her out. The Blonde looks back at her, and the cadet can tell that the trooper approves of what she sees, as her eyes take in the long black hair, pert young breasts and luscious shaved mound of Venus. Yes, she thinks I'm pretty too, the cadet realizes. She locks eyes with the Blonde, and sees something new and even deeper in the eyes that stare back into hers. It is an unmistakable glint of deep seated cruelty. Yes, she is going to take my life, and she is going to enjoy doing it, the cadet realizes. She suddenly flushes deeply, and drops her eyes demurely in embarrassment. What's happening to me? she asks herself in confusion. My pussy is getting wet! Can she possibly be excited at the prospect of her own death at the hands of this beautiful woman? She shyly raises her eyes, and can detect the slightest trace of a satisfied smirk on the Blonde's lips. Yes, she knows, realizes the cadet. "Ready!" rings out the voice of the corporal. The troopers raise their rifles, bayonets pointed at the bellies of the cadets. "On my command! One! Two! Three! Thrust!"
Both troopers lunge with their bayonets. The taller trooper gives a straightforward thrust into the belly of her cadet, burying the bayonet in her up to the hilt, and forcing an agonized gasp out of her victim. She then gives the bayonet a half twist, playing lethal havoc with the young guts that it slashes open. The petite trooper, maintaining unbroken eye contact with her cadet, slices into the soft young flesh with an upward thrust of her bayonet. The cadet does not break eye contact with her killer. She opens her mouth and gasps in agony, but masters herself and does not cry out. Yes, she wants me to suffer, the cadet realizes. And I must suffer, because my life has only been preparation for this moment. The pain increases to unbearable proportions as the Blonde pushes the barrel of the rifle upward, carving deeper into the ripe young flesh. The cadet feels her feet begin to lift off the ground, as the Blonde forces her onto her tiptoes. Yes, she is taking my life, but by taking my life, she will be making me a part of her, the cadet philosophizes in an effort to block out the unbelievable pain. The cadet begins to pant in agony as she is held up on her tiptoes for what seems like an eternity. The Blonde corporal, looking at her watch, determines that the prisoners have suffered through their regulation minute. "Withdraw!" she shouts. The taller trooper pulls her rifle straight back, sliding the blade out of her cadet. Eyes rolling back in her head, the girl thumps heavily face down onto the ground at the trooper's feet. The petite trooper slowly lowers her cadet back down until her feet are once again flat on the ground and then pulls out her bayonet. The cadet can now feel the life literally drain out of her as she watches the red deluge flow from her devastated belly. Blackness begins to close in on her as she drops to her knees. Her breath now comes in quick little gasps. As from a distance she hears what sounds like a sob from the body lying off to her side, and then silence. I will be with you soon, my friend, she thinks, as she flops onto the ground on her ruined belly. She can feel the warmth and wetness beneath her grow, as her wide open eyes stare at the Blonde trooper's boots. I won't close my eyes, death will do that for me. The blood should make me feel warm, but now I'm starting to get cold. Why is that? she asks as the eternal darkness shuts down her brain and enfolds her in its embrace.
Two more bayonet thrusts and the two captured infantrywomen are skewered on Blonde bayonets. Soon, the cadet, her eyes wide open and her pretty little toes with their pink toenails pointing skyward, is lying in a trench sandwiched between her cadet friend and one of the infantrywomen. Twenty two young women in all fill this slit in the hungry earth. Soon, they will be lost to sight as their common grave is filled in and their once luscious flesh becomes nothing more than food for worms.
"Look at these heels! And the lacy undies! And this little slut was wearing a thong!" marvels Jan, looking at the discarded finery of the two slain cadets. "And did you see? They both had painted toenails! They really pamper those cadets!" exclaims Donna. "You and Janine really did a job on those girls!" Debbie chimes in enthusiastically. "We sure did!" Donna smiles proudly. "I made both of my little sweeties feel it, especially that cadet," Janine purrs with a cruel smirk. "I sure miss wearing heels!" Jan remarks wistfully. "Me too," agrees Donna. "We probably wouldn't fit in these. They do have smaller feet than we do." "Hey, Janine, you and Michelle should try on these heels! You're both really small girls," suggests Jan. As the other troopers look on, the two petite blondes pull off their boots and slip their feet into the now ownerless high heels. "They fit great," Janine affirms, wriggling her toes in the shoes of the girl she had snuffed out mere moments before. "Yeah, they're actually pretty nice heels," agrees Michelle. "You should try on their undies, too," Donna suggests mischievously. "No, thanks!" replies Janine. "It's bad enough I'm wearing shoes that had another girl's feet in them. Do you know what was in those panties?" All five troopers laugh uproariously.
Darkness is now falling. "So, are we pulling out tonight, sarge?" Katie asks Amy. " I can't believe they haven't counterattacked us yet. We were taking an awful chance staying here." "We're not pulling out, corporal," replies Amy. "Our orders are to hold this position at all costs. We should be getting reinforcements tomorrow." "So this could be a major battle, then?" Katie asks in an almost awed tone. "Headquarters is going to throw a lot of women into here to defend this place, and you can be sure the enemy is going to throw a lot of women at us to get it back", Amy responds. "I'm sorry I didn't tell you about this earlier, but Karen and I were under orders to maintain strict secrecy," Amy continues apologetically. "No problem, sarge. We all gotta do what we gotta do," Katie answers reassuringly.
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4 comments
anonymous reader
2013-07-15 00:39:04
I 100% agree with the little sister comment. They are evil succubae that suck the soul out of you and would slit your throat without a second thought just like the unfortunate sleeping platoon in the story.
anonymous reader
2013-03-24 08:53:34
Good work indeed. I wish to read other parts of those stories, other bayonets in naked female bellies, for I have a serious belly fetish. :-)
anonymous reader
2011-12-08 17:48:59
anyone that has a little sister knows how soulless a female can be, so I KNOW how much MORE bloody the world would be if it was ran by women
anonymous reader
2011-12-08 12:06:36
Not really a sex story, but you are a good writer nontherless
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